Partners in crime: Autoantibodies complicit in COVID‐19 pathogenesis

Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the dev...

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Published inReviews in medical virology Vol. 33; no. 2; pp. e2412 - n/a
Main Authors Taghadosi, Mahdi, Safarzadeh, Elham, Asgarzadeh, Ali, Roghani, Seyed Askar, Shamsi, Afsaneh, Jalili, Cyrus, Assar, Shirin, Soufivand, Parviz, Pournazari, Mehran, Feizollahi, Parisa, Nicknam, Mohammad Hossein, Asghariazar, Vahid, Vaziri, Siavash, Shahriari, Hossein, Mohammadi, Asadollah
Format Journal Article
LanguageEnglish
Published England Wiley Periodicals Inc 01.03.2023
John Wiley and Sons Inc
Subjects
Autoantibodies
autoantibody (AAB)
Autoimmune diseases
Autoimmunity
Cell activation
Child
Complications
COVID-19
Crime
Cytokine storm
Cytokines
Environmental factors
Humans
Inflammation
Leukocytes (neutrophilic)
Multisystem inflammatory syndrome in children
Neutrophils
Pathogenesis
Post-Acute COVID-19 Syndrome
Respiratory distress syndrome
Review
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
Thrombosis
COVID-19
SARS-CoV-2
autoimmunity
autoantibody (AAB)
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Abstract Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID‐19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID‐19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll‐like receptor‐7 (TLR‐7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS‐CoV‐2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS‐CoV‐2 by disrupting cytokine function and triggering neutrophil hyper‐reactivity. Finally, the pathologic effects of these AABs will be further described in COVID‐19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS‐C), acute respiratory distress syndrome (ARDS), and recently described post‐acute sequelae of COVID‐19 (PASC) or long‐COVID.
AbstractList Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID-19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID-19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll-like receptor-7 (TLR-7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS-CoV-2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS-CoV-2 by disrupting cytokine function and triggering neutrophil hyper-reactivity. Finally, the pathologic effects of these AABs will be further described in COVID-19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS-C), acute respiratory distress syndrome (ARDS), and recently described post-acute sequelae of COVID-19 (PASC) or long-COVID.
Abstract Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID‐19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID‐19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll‐like receptor‐7 (TLR‐7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS‐CoV‐2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS‐CoV‐2 by disrupting cytokine function and triggering neutrophil hyper‐reactivity. Finally, the pathologic effects of these AABs will be further described in COVID‐19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS‐C), acute respiratory distress syndrome (ARDS), and recently described post‐acute sequelae of COVID‐19 (PASC) or long‐COVID.
Author Shamsi, Afsaneh
Soufivand, Parviz
Feizollahi, Parisa
Assar, Shirin
Vaziri, Siavash
Asghariazar, Vahid
Safarzadeh, Elham
Jalili, Cyrus
Nicknam, Mohammad Hossein
Asgarzadeh, Ali
Roghani, Seyed Askar
Taghadosi, Mahdi
Pournazari, Mehran
Shahriari, Hossein
Mohammadi, Asadollah
AuthorAffiliation 7 Department of Immunology School of Medicine Tehran University of Medical Sciences Tehran Iran
12 Cellular and Molecular Research Center Research Institute for Health Development Kurdistan University of Medical Sciences Sanandaj Iran
2 Department of Microbiology, Parasitology, and Immunology Ardabil University of Medical Sciences Ardabil Iran
3 Students Research Committee School of Medicine Ardabil University of Medical Sciences Ardabil Iran
8 Molecular Immunology Research Centre Tehran University of Medical Sciences Tehran Iran
4 Medical Biology Research Center Health Technology Institute Kermanshah University of Medical Sciences Kermanshah Iran
9 Deputy of Research and Technology Ardabil University of Medical Sciences Ardabil Iran
11 Clinical Immunology Research Center Zahedan University of Medical Sciences Zahedan Iran
10 Infectious Disease Research Center Kermanshah University of Medical Sciences Kermanshah Iran
5 Clinical Research Development Center Imam Reza Hospital Kermanshah Universit
AuthorAffiliation_xml – name: 5 Clinical Research Development Center Imam Reza Hospital Kermanshah University of Medical Sciences Kermanshah Iran
– name: 9 Deputy of Research and Technology Ardabil University of Medical Sciences Ardabil Iran
– name: 1 Immunology Department Faculty of Medicine Kermanshah University of Medical Sciences Kermanshah Iran
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– name: 6 Department of Anatomy Kermanshah University of Medical Sciences Kermanshah Iran
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– name: 3 Students Research Committee School of Medicine Ardabil University of Medical Sciences Ardabil Iran
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Keywords COVID-19
SARS-CoV-2
autoimmunity
autoantibody (AAB)
Language English
License 2022 John Wiley & Sons Ltd.
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Snippet Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these...
Abstract Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in...
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SubjectTerms Autoantibodies
autoantibody (AAB)
Autoimmune diseases
Autoimmunity
Cell activation
Child
Complications
COVID-19
Crime
Cytokine storm
Cytokines
Environmental factors
Humans
Inflammation
Leukocytes (neutrophilic)
Multisystem inflammatory syndrome in children
Neutrophils
Pathogenesis
Post-Acute COVID-19 Syndrome
Respiratory distress syndrome
Review
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
Thrombosis
Title Partners in crime: Autoantibodies complicit in COVID‐19 pathogenesis
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Frmv.2412
https://www.ncbi.nlm.nih.gov/pubmed/36471421
https://www.proquest.com/docview/2785187103
https://pubmed.ncbi.nlm.nih.gov/PMC9877745
Volume 33
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